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TTLL12 counteracts BPOZ-2 to stabilize eEF1A1 and promote hepatocarcinogenesis

Kaiming Leng1,2, Zhen Yang3, Yao Liming1,2

  • 1Department of Hepatopancreatobiliary Surgery, Qingdao Municipal Hospital, Qingdao University, Qingdao, PR China.

Cell Death & Disease
|April 21, 2026
PubMed

Insights

Tubulin tyrosine ligase-like enzyme-12 (TTLL12) is highly expressed in liver cancer (HCC), promoting tumor growth. TTLL12 protects eEF1A1 from degradation, offering a new therapeutic target for HCC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Tubulin tyrosine ligase-like enzyme-12 (TTLL12) is involved in posttranslational tubulin modifications and cancer development.
  • The specific role and mechanisms of TTLL12 in hepatocellular carcinoma (HCC) are not fully understood.

Purpose of the Study:

  • To investigate the expression, function, and mechanism of TTLL12 in hepatocellular carcinoma (HCC).
  • To evaluate TTLL12 as a potential therapeutic target for HCC.

Main Methods:

  • Analysis of TTLL12 expression in HCC tissues and adjacent normal tissues.
  • In vitro functional assays (cell proliferation, oncogenic behaviors) involving TTLL12 knockdown and overexpression.
  • In vivo tumor growth models using TTLL12-overexpressing cells.
  • Mechanistic studies involving eEF1A1, Bood POZ-containing gene type 2 (BPOZ-2), and CULLIN (CUL3) pathways.

Main Results:

  • TTLL12 expression is significantly elevated in HCC tissues and correlates with poor prognosis.
  • Knockdown of TTLL12 inhibits HCC cell proliferation, while overexpression promotes oncogenic behaviors and tumor growth in vivo.
  • TTLL12 suppresses the ubiquitin-proteasome degradation of eEF1A1 by competing with BPOZ-2 for CUL3 recruitment.
  • This mechanism enhances cancer cell proliferation in HCC.

Conclusions:

  • TTLL12 exhibits oncogenic potential in hepatocarcinogenesis by stabilizing eEF1A1.
  • TTLL12 represents a novel therapeutic target for hepatocellular carcinoma (HCC).

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